In the present study we evaluated the modulation of the sarcolemmal ATP sensitive K+ channel by insulin. The "in vivo" administration of insulin to the rats led to an hyperpolarization of the skeletal muscle fibers. This effect is antagonized by "in vitro" incubation of the muscle with glybenclamide, an ATP sensitive K+ channel blocker. Patch clamp experiments revealed that insulin enhanced the mean current of the ATP sensitive K+ channel by a factor of 1.4. This effect is mediated by an increase of the channel open probability, while no change occurred in the single channel conductance nor in the channel density. In the treated rats, the sensitivity of the channel to ATP and glybenclamide is abnormally reduced. Our results are consistent with an activation of the ATP sensitive K+ channel by insulin. This contributes to the hyperpolarization of the skeletal muscle fibers.

In the present study we evaluated the modulation of the sarcolemmal ATP sensitive K+ channel by insulin. The "in vivo" administration of insulin to the rats led to an hyperpolarization of the skeletal muscle fibers. This effect is antagonized by "in vitro" incubation of the muscle with glybenclamide, an ATP sensitive K+ channel blocker. Patch clamp experiments revealed that insulin enhanced the mean current of the ATP sensitive K+ channel by a factor of 1.4. This effect is mediated by an increase of the channel open probability, while no change occurred in the single channel conductance nor in the channel density. In the treated rats, the sensitivity of the channel to ATP and glybenclamide is abnormally reduced. Our results are consistent with an activation of the ATP sensitive K+ channel by insulin. This contributes to the hyperpolarization of the skeletal muscle fibers.